Superior mesenteric artery syndrome and acute pancreatitis in a boy with eating disorder: a case report

Abstract

Eating disorders are an important cause of physical and psychosocial disturbances. Gastrointestinal complications in eating disorders are common and include pancreatitis and superior mesenteric artery syndrome (SMAS). However, only two patients who simultaneously suffered from both SMAS and pancreatitis in the setting of an eating disorder have ever been reported in the literature. We describe here a patient with eating disorder not otherwise specified (ED-NOS) who exhibited both SMAS and pancreatitis concomitantly. An 11-year-old boy with ED-NOS had presented with the sudden onset of recurrent bilious vomiting, abdominal distension and abdominal pain. Laboratory and imaging studies revealed that the patient had SMAS and acute pancreatitis. Gastric decompression and intravenous infusion of fluids promptly improved his abdominal symptoms and laboratory data. This is the first case report of a patient with ED-NOS who simultaneously suffered from SMAS and pancreatitis in the pediatric literature. Since SMAS and pancreatitis can both cause patients to be severely ill, these diseases should be considered in patients with eating disorders who exhibit abdominal symptoms such as vomiting or abdominal pain.

Food Insecurity Leading to Superior Mesenteric Artery Syndrome Managed Successfully with Endoscopic Gastrojejunostomy Stent

“…The most well-accepted proposed pathophysiologic mechanism is that duodenal compression by the SMA causes secondary post-papillary syndrome and retrograde reflux of bile into the pancreatic duct, resulting in inflammation [ 18 ]. At least 1 previous case noted improvement in a patient’s symptoms and serum amylase level after decompression of the distended proximal bowel, supporting the idea that increased intraluminal pressure in the duodenum can lead to high pancreatic duct pressures [ 22 ].…”

“…The rapid improvement in this patient’s acute cholestatic lab values in the first 24 hours without intervention supported the suspicion that this represented transient biliary stasis (eg, passage of biliary stone or sludge, duodenal compression by the SMA). Regarding the latter mechanism, SMA syndrome-associated acute pancreatitis has been reported in the literature, albeit rarely [ 15 – 22 ]. The most well-accepted proposed pathophysiologic mechanism is that duodenal compression by the SMA causes secondary post-papillary syndrome and retrograde reflux of bile into the pancreatic duct, resulting in inflammation [ 18 ].…”